OBJECTIVE: To determine the relationship between the blood serum brain-derived neurotrophic factor (BDNF) level and cognitive function deterioration in patients with obstructive sleep apnea/hypopnea syndrome (OSAHS), and to explore the possible mechanism of cognitive impairment. METHODS: Twenty-eight male OSAHS patients and 14 normal males (as controls) were enrolled in the study. Polysomnography and the Montreal cognitive assessment (MoCA) were conducted. The blood serum BDNF levels were measured using ELISA. RESULTS: The OSAHS group had significantly decreased blood serum BDNF levels compared with the control group (t = -10.912, P = 0.000). The blood serum BDNF level of the subjects was significantly positively associated with the MoCA score (r = 0.544, P = 0.000), significantly negatively associated with the apnea-hypopnea index (AHI) and shallow sleep (S1+S2) (AHI: r = -0.607, P = 0.000; S1+S2: r = -0.768, P = 0.000), and significantly positively associated with the lowest SaO(2) (LSO), slow wave sleep (S3+S4), and rapid eye movement sleep (REM) (LSO: r = 0.566, P = 0.000; S3+S4: r = 0.778, P = 0.000; REM: r = 0.575, P = 0.000). CONCLUSIONS: OSAHS patients have significantly decreased blood serum BDNF levels compared with the control. Nocturnal hypoxia as well as the deprivation of slow wave sleep and REM may lead to the decreased serum BDNF level of OSAHS patients. This decreased blood serum BDNF level may contribute to the cognitive impairment in OSAHS.
OBJECTIVE: To determine the relationship between the blood serum brain-derived neurotrophic factor (BDNF) level and cognitive function deterioration in patients with obstructive sleep apnea/hypopnea syndrome (OSAHS), and to explore the possible mechanism of cognitive impairment. METHODS: Twenty-eight male OSAHS patients and 14 normal males (as controls) were enrolled in the study. Polysomnography and the Montreal cognitive assessment (MoCA) were conducted. The blood serum BDNF levels were measured using ELISA. RESULTS: The OSAHS group had significantly decreased blood serum BDNF levels compared with the control group (t = -10.912, P = 0.000). The blood serum BDNF level of the subjects was significantly positively associated with the MoCA score (r = 0.544, P = 0.000), significantly negatively associated with the apnea-hypopnea index (AHI) and shallow sleep (S1+S2) (AHI: r = -0.607, P = 0.000; S1+S2: r = -0.768, P = 0.000), and significantly positively associated with the lowest SaO(2) (LSO), slow wave sleep (S3+S4), and rapid eye movement sleep (REM) (LSO: r = 0.566, P = 0.000; S3+S4: r = 0.778, P = 0.000; REM: r = 0.575, P = 0.000). CONCLUSIONS: OSAHS patients have significantly decreased blood serum BDNF levels compared with the control. Nocturnal hypoxia as well as the deprivation of slow wave sleep and REM may lead to the decreased serum BDNF level of OSAHS patients. This decreased blood serum BDNF level may contribute to the cognitive impairment in OSAHS.